کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8479173 | 1551292 | 2015 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Acetylation and phosphorylation of STAT3 are involved in the responsiveness of microglia to beta amyloid
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کلمات کلیدی
STAT3AβAPPTLRCcl5RAGEchemokine (C–C motif) ligand 5JAKs - JAKSAlzheimer's disease - بیماری آلزایمرMicroglia - میکروگلیاهاamyloid precursor protein - پروتئین پیش ماده آمیلوئیAmyloid beta peptides - پپتیدهای بتا آمیلئیدJanus kinases - ژنوس کینازReceptor for advanced glycation end products - گیرنده برای محصولات پیشرفته glycation پایانToll-like receptors - گیرنده های پولی مانند
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Microglia are macrophages within the central nervous system playing a central role in neurodegenerative disorders. Although the initial engagement of microglia seems to be neuroprotective, many lines of evidence indicate that its persistent activation contributes to dismantle neuronal activity and to induce neuronal loss. The molecular pathways that lead from amyloid interaction with membrane receptors to the microglial activation have been extensively investigated, although a definitive picture is not yet at hand. In this work, primary and immortalized microglial cells were treated with a synthetic form of Aβ peptides, and relative abundance of acetylated and phosphorylated STAT3 were assayed. Results highlight, for the first time, three distinctive sequential events: i) an earlier event marked by the increase in the level of STAT3 acetylated species, followed by ii) a later increase in the level of STAT3 phosphorylated form, and finally iii) an involvement of phosphorylated STAT3 in the increase in expression of the 14-3-3 epsilon, a protein frequently associated with neurodegenerative diseases and known to be a marker of Aβ-activated microglia. These data outline a complex, time-dependent modification of STAT3 signalling triggered by amyloid in the microglial compartments, that once confirmed by in vivo experiments will broaden the knowledge of the molecular basis of amyloid neurotoxicity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 81, February 2015, Pages 48-56
Journal: Neurochemistry International - Volume 81, February 2015, Pages 48-56
نویسندگان
Margherita Eufemi, Rossana Cocchiola, Donatella Romaniello, Virginia Correani, Laura Di Francesco, Cinzia Fabrizi, Bruno Maras, M. Eugenia Schininà ,